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Giovanni Solinas

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Associate Professor of Biochemistry

Link Campus University

Italy

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About

Giovanni Solinas is a Professor at the University of Gothenburg, Sweden. His research areas focus on insulin biology, diabetes, obesity, and associated metabolic disorders. Recent articles include studies on insulin-induced lipohypertrophy, PI3K inhibitors, and the role of adipocytes in insulin secretion. His work aims to unravel the complex interactions between metabolic signaling and disease.

Recent Grants

Grant: Open

Developing Optimal PI3K-targeted Cancer Therapies from a Better Understanding of the Insulin System

Open Date: 2024-01-01

Close Date: 2026-12-01

Grant: Close

Mechanistic characterization of the adiposecretin effect: a novel paradigm for the insulin system to treat obesity-driven diabetes

Open Date: 2023-06-01

Close Date: 2026-06-01

Grant: Open

Defining Feedback Loops Between Phosphoinositide 3-kinases (PI3Ks) Isoforms and Insulin to Harness the Full Potential of PI3K-Targeted Therapies

Open Date: 2023-01-01

Close Date: 2026-12-01

Grant: Close

Defining the Role of PI3K Isoforms in Adipose Tissue Lipolysis and Thermogenesis to Treat Obesity with Isoform-Selective PI3K Inhibitors

Open Date: 2022-01-01

Close Date: 2024-01-01

Grant: Close

Resolving the Role of Specific Phosphoinositide 3-kinases (PI3Ks) Isoforms in Metabolism-Insulin Loops Driving Tumor-Promotion

Open Date: 2021-01-01

Close Date: 2023-12-01

Articles (17)

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2026

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2022

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2022

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2022

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2021

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2021

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2020

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2020

Collaborators (5)

Maria Johansson

Senior Lecturer

University of Gothenburg

SWEDEN

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Per-Anders Jansson

Professor

University of Gothenburg

SWEDEN

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Johan Ruud

Assistant Professor, Senior Lecturer

University of Gothenburg

SWEDEN

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Damien RAMEL

FRANCE

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Robert Häsler

Professor of Systems Medicine in Dermatology

Christian-Albrechts-Universität zu Kiel

GERMANY

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Giovanni Solinas

Research Interests

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About

Recent Grants

Articles (17)

Loss of hepatocyte PI3Kα reduces hepatocellular carcinoma and hepatocyte proliferation in association with altered lipid metabolism

Harnessing insulin biology to treat diabetes and cancer

Prevention of insulin-induced lipohypertrophy by coadministration of a low dose of high-affinity PI3K inhibitors

Ablation of PI3Kγ in neurons protects mice from diet-induced obesity MASLD and insulin resistance

Insulin Hypersecretion as Promoter of Body Fat Gain and Hyperglycemia.

An adipoincretin effect links adipostasis with insulin secretion

Activation of GFRAL<sup>+</sup> neurons induces hypothermia and glucoregulatory responses associated with nausea and torpor.

Activation of GFRAL plus neurons induces hypothermia and glucoregulatory responses associated with nausea and torpor

Adipocyte PI3K links adipostasis with baseline insulin secretion at fasting through an adipoincretin effect

Adipocyte PI3K links adipostasis with baseline insulin secretion at fasting through an adipoincretin effect

PI3K and AKT at the Interface of Signaling and Metabolism.

Somatic ablation of IKKβ in liver and leukocytes is not tolerated in obese mice but hepatic IKKβ deletion improves fatty liver and insulin sensitivity

Tubular IKKβ Deletion Alleviates Acute Ischemic Kidney Injury and Facilitates Tissue Regeneration

PI3Kγ promotes obesity-associated hepatocellular carcinoma by regulating metabolism and inflammation

Hyperinsulinemia and insulin resistance in the obese may develop as part of a homeostatic response to elevated free fatty acids: A mechanistic case-control and a population-based cohort study.

JNK1 ablation improves pancreatic β-cell mass and function in db/db diabetic mice without affecting insulin sensitivity and adipose tissue inflammation.

Insulin signaling and glucose metabolism in different hepatoma cell lines deviate from hepatocyte physiology toward a convergent aberrant phenotype.

Collaborators (5)

Maria Johansson

Per-Anders Jansson

Johan Ruud

Damien RAMEL

Robert Häsler

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